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Metabolic diseases, inherited: Also called inborn errors of metabolism, these are heritable (genetic) disorders of biochemistry. Research by scientists from Oxford University and the University of Exeter in Britain into the genetic origins of disease, funded by the Wellcome Trust and published Friday in Science, led to the discovery of the FTO gene. For this research, the genomes of 2,000 people with type 2 diabetes were compared with the genomes of 3,000 healthy individuals. Fifty percent of people are likely to carry one high-risk copy and one low-risk, putting them at a 30-percent greater vulnerability of developing obesity. The extra weight in each case was found to come neither from greater height nor from developed muscle but exclusively from extra body fat. The scientists point out that FTO is not the only gene that will have an impact on obesity. This news will come as a relief to people who pay attention to their diet -- and who cannot understand with their eating and exercise habits why they should be carrying extra weight -- that their genes may be responsible.
So in this spring season when there's no reason to bypass the produce aisles and head for the ready-made food shelves in the supermarket, think green.
Out shopping, grab bunches of vegetables that are in their infancy, like broccolini, the smallest french beans, snow peas and more, and steam them just until they've lost their stiffness and still have a bit of crunch.
Then toss them in a glug of excellent olive oil and sprinkle with a pinch of sea salt and freshly ground black pepper.
For the protein, per serving lay two slices of prosciutto ham, then a 4-ounce fillet of firm white fish on a piece of greaseproof paper large enough to wrap around and enclose it.
Put a couple of fresh springs of tarragon on top and two or three thin slices of lemon on that, season to taste, then bring any of the ham round and over the fillet, fold up the paper tightly to close, then microwave for 4 minutes for a 1-inch thick fillet, or until opaque.
Serve on top of a mixed mound of the steamed vegetables and relish the flavor and the start of a new way of life. Mendelian inheritance is a term sometimes used to describe patterns of inheritance, based on the original ideas of dominant and recessive genes, first proposed by the Gregorian Monk Mendel. In autosomal dominant inheritance, the affected individual will have one ‘good’ copy of the gene, and one ‘bad’ copy. This is contrary to autosomal recessive conditions, where to be affected, an individual has to be homozygous for a particular gene (they have to have two ‘bad copies’). Punnett’s square is an easy way to determine the risk of an affected individual passing on the risk to their child.
An affected parent typically has a 50% chance of passing on the defect to any of their offspring.
Pleiotropy – this is the ability of an affected gene to cause two or more seemingly unrelated clinical effects. Variable Expressability – even within the same family, an inherited genetic defect can cause massively different degrees of clinical effect. Reduced penetrance – this is the phenomenon whereby an individual in the family may carry the autosomal dominant gene but may not show any clinical features.
Somebody who is heterozygous for a defective gene but has no clinical features is said to be reperesent non-penetrance.
Codominance – this is where two dominant states are expressed simultaneously in the same individual. The risk of having an affected child when both parents are carriers is 25%, and the chance of having a child who is a carrier is 50%.
If one parent is homozygous, and one is only a carrier, then they have a 50% chance of having an effected child.

Consanguinity  (parents are related; Generally the risk is higher the more closely the parents are related) increases the risk of having an affected child – as it increases the risk that both parents carry an affected gene.
Locus heterogeneity – this refers to the phenomenon whereby there may be more than one recessive gene that accounts for a particular condition.
A disorder where the same phenotype can result from different mutations is known as a genocopy.
Mutational heterogeneity – this is the phenomenon whereby there are different mutations, but at the same loci. Often the family history is weak (there is often gonadal mosaicism, and few affected relatives). Despite a weak family history, genetic testing and counselling can be necessary, as all carrier females have a 50% risk of having an affected son, whoever their partner is.
Sometimes called ‘Knight’s move’ inheritance – as it apparently skips generations, and presents with unusual pedigree patterns.
Mitochondrial DNA is only passed on through the mother – only the oocyte contain mitochondrial DNA and not the sperm.
For some genes, the copy received from one parent has different activity to the copy received from the other parent. Thus the child must inherit the active gene from the father inorder to be free of the disease.
There are many disorders for which there are many environmental and genetic factors at play that account for an individual’s overall risk of contracting the disease. In such conditions, the exact genetic makeup is usually complex, and cannot be accounted for by a specific gene, however, there will often be a family history of the condition(s) to which the child is more susceptible. Genes that make you susceptible to a condition increase your risk of contracting the condition, but don’t necessarily mean you will get it.
Diseases such as type 2 diabetes, Crohn’s disease and even smoking addiction has been passed on to us by our ancestors. Researchers have discovered that the modern human population carries more than a fifth of archaic Neanderthal human DNA.
The two separate human subspecies co-existed on earth thousands of years ago, until the Neanderthals became extinct around 30.000 years ago.
This finding allows scientists to study over 20% of the Neanderthals genomes without having to extract the genetic material from fossils. The researchers found that non-Africans carried 1 to 3% Neanderthal DNA, but the total amount in current humans reached about 20%. The Neanderthal genes that live on today, make keratin and protein used for the skin, nails and hair. Professor Chris Stringer, a leading expert in human origins at London’s Natural History Museum said the findings added a twist to the debate about how early humans related to the Neanderthals. Examples include albinism, cystinuria (a cause of kidney stones), phenylketonuria (PKU), and some forms of gout, sun sensitivity, and thyroid disease. It's the main cause of heart disease, type 2 diabetes and cancer and has been described as a greater danger than smoking, alcohol and poverty. They established that particular versions of FTO appeared more frequently among people with type 2 diabetes. They were found to have two copies of the high-risk version and to carry an average of 7 pounds excess weight, with 15 percent more body fat. Nor does inheriting a variant of the gene automatically mean that a person will become overweight.

It would be a mistake for anyone carrying more body fat than they should to persist in their present poor habits while waiting for some drug to come along that will magically make them thin and healthy. Drawing out the ‘family tree’ and highlight affected individuals is a good way of noting down a lot of information without having to write much, and also makes the pattern easier to spot. For example, don’t let an instance of non-penetrance confuse you into thinking it is not autosomal dominant!
A simple example is an individual of AB blood type, who expressed both group A and group B proteins. In reality, the vast majority of autosomal recessive cases will be due to mutational heterogeneity, and perhaps a small proportion will be truly homogeneic, particularly in consanguineous couples.
Each cell has 1,000 copies of mitochondrial DNA, but typically, only a proportion of the mitochondrial DNA is affected. Thus fathers with mitochondrial DNA disorders will not pass the defect onto their children.
Neanderthals have been dead for tens of thousands of years, but their genetic code still lives on. Scientists have compared genetic variants of the DNA of 176 people from sub-saharan Africa, a toe bone from a 50,000 year old Neanderthal woman and 846 people from non-African heritage.
These are only a very few of the hundreds of known inborn errors of metabolism. Advances in the diagnosis and treatment of inborn errors of metabolism have improved the outlook for many of these conditions so that early diagnosis, if possible in infancy, can be helpful.
With the lowest danger of becoming obese are the 34 percent of people who have two low-risk copies. In such cases, often two deaf individuals will have children together, you would expect that this would mean they had a 100% chance of having an affected child, but many children are born with normal hearing. The Y chromosome is typically only associated with spermatogenesis, and thus any conditions involving Y-linked inheritance will typically result in infertility. Failure to receive the gene can be due to a de novo deletion, or it can be the result of Uniparental disomy – where two copies of one gene are received from the same parent. We were one of the first groups to identify the role of the phospholamban gene in determining QT interval in the general population and showed that a combined risk score using 11 of the QT-associated loci only explain about 10% of the heritability of QT. Curious as to whether FTO had an influence upon obesity, they tested their hypothesis on a vastly increased sample of 37,000 people. There is a massive -- the word is deliberately chosen -- difference between 7 pounds excess weight and 20, 50 and 100-plus pounds excess weight. This is because the affected parents have different mutations at different loci – and thus the mutations can be treated as separate, and thus it is as if only one parent is affected.
We are now involved in a much larger collaboration – the QT Interval International Consortium of Genome-wide Association Studies (QT-IGC). We have previously shown that NOS1AP gene variants play a role in modulating QT intervals in healthy subjects, and other groups have shown that severity of presentation in LQTS is also modulated by NOS1AP variants. We have recently identified common variants in 22 loci, which are associated with QRS duration and cardiac ventricular conduction. As part of the Cardiovascular Trait Consortium we have been able to nominate a list of genes we are most interested in working on, mostly selected based on published and unpublished Genome Wide Association Studies (GWAS) for which mutant mice will be made at Harwell.

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  1. QaRa_BaLa

    Photograph and textual content from the before.


  2. PaTRoN

    Scientific evidence supporting it, as well as my own experience trying to help people insulin.